Acute viral gastroenteritis induced by Norwalk and Hawaii agents results in a marked, but transient, lymphopenia at the height of illness, which involves all lymphocyte subpopulations (T, B, and null cells). The lymphocytes remaining in the circulation respond normally to mitogens. This lymphopenia may be a result of an acute redistribution of circulating lymphocytes to sites of infection in the gut. Infection with the Hawaii agent is associated with a serum antibody rise to the Hawaii particle as measured by immune electron microscopy, along with a spectrum of clinical illness and histopathologic responses. Experimental infection in man with Udorn and Georgia strains of influenza virus (H3N2) resulted in a mild lymphopenia, with a mild suppression of lymphocyte responsiveness to mitogens. Low levels of specific antigen stimulation were seen in 4 week convalescent lymphocyte cultures. Polymorphonuclear leukocyte function appeared to be normal during influenza, but phagocytosis-stimulated Cl-glucose oxidation appeared to be decreased during viral gastroenteritis.